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The irreducible complex system of the eye, and eye-brain interdependence

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The irreducible complex system  of the eye, and eye-brain interdependence

http://reasonandscience.heavenforum.org/t1638-the-irreducible-complex-system-of-the-eye-and-eye-brain-interdependence

The signal transduction pathway is irreducible complex  4

http://www.detectingdesign.com/humaneye.html

The first step in vision is the detection of photons. 5  In order to detect a photon, specialized cells use a molecule called 11-cis-retinal.  When a photon of light interacts with this molecule, it changes its shape almost instantly.  It is now called trans-retinal.  This change in shape causes a change in shape of another molecule called rhodopsin.  The new shape of rhodopsin is called metarhodopsin II.  Metarhodopsin II now sticks to another protein called transducin forcing it to drop an attached molecule called GDP and pick up another molecule called GTP.  The GTP-transducin-metarhodopsin II molecule now attaches to another protein called phosphodiesterase.  When this happens, phosphodiesterase cleaves molecules called cGMPs.  This cleavage of cGMPs reduces their relative numbers in the cell.  This reduction in cGMP is sensed by an ion channel.  This ion channel shuts off the ability of the sodium ion to enter the cell.  This blockage of sodium entrance into the cell causes an imbalance of charge across the cell's membrane.  This imbalance of charge sends an electrical current to the brain.  The brain then interprets this signal and the result is called vision.

Many other proteins are now needed to convert the proteins and other molecules just mentioned back to their original forms so that they can detect another photon of light and signal the brain.  If any one of these proteins or molecules is missing, even in the simplest eye system, vision will not occur.

The question now of course is, how could such a system evolve gradually?  All the pieces must be in place simultaneously.  For example, what good would it be for an earthworm that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or "spot" of cells on its head?  These cells now have the ability to detect photons, but so what?  What benefit is that to the earthworm?  Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them.  So what?!  What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to the worm's minute brain?   Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the worm's brain.  So what?!  How is the worm going to know what to do with this signal?  It will have to learn what this signal means.  Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems.  Now the earthworm, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring.  If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them.  All of these wonderful processes need regulation.  No function is beneficial unless it can be regulated (turned off and on).  If the light sensitive cells cannot be turned off once they are turned on, vision does not occur.  This regulatory ability is also very complicated involving a great many proteins and other molecules - all of which must be in place initially for vision to be beneficial.

Photoreceptor cells point to intelligent design
http://reasonandscience.heavenforum.org/t1696-photoreceptor-cells-point-to-intelligent-design

How the origin of the human eye is best explained through intelligent design  
http://reasonandscience.heavenforum.org/t2411-how-the-origin-of-the-human-eye-is-best-explained-through-intelligent-design

Signal transduction pathway

The absorption of light leads to an isomeric change in the retinal molecule.
The signal transduction pathway is the mechanism by which the energy of a photon signals a mechanism in the cell that leads to its electrical polarization. This polarization ultimately leads to either the transmittance or inhibition of a neural signal that will be fed to the brain via the optic nerve. The steps, or signal transduction pathway, in the vertebrate eye's rod and cone photoreceptors are then:

1.The rhodopsin or iodopsin in the disc membrane of the outer segment absorbs a photon, changing the configuration of a retinal Schiff base cofactor inside the protein from the cis-form to the trans-form, causing the retinal to change shape.
2.This results in a series of unstable intermediates, the last of which binds stronger to the G protein in the membrane and activates transducin, a protein inside the cell. This is the first amplification step – each photoactivated rhodopsin triggers activation of about 100 transducins. (The shape change in the opsin activates a G protein called transducin.)
3.Each transducin then activates the enzyme cGMP-specific phosphodiesterase (PDE).
4.PDE then catalyzes the hydrolysis of cGMP to 5' GMP. This is the second amplification step, where a single PDE hydrolyses about 1000 cGMP molecules.
5.The net concentration of intracellular cGMP is reduced (due to its conversion to 5' GMP via PDE), resulting in the closure of cyclic nucleotide-gated Na+ ion channels located in the photoreceptor outer segment membrane.
6.As a result, sodium ions can no longer enter the cell, and the photoreceptor outer segment membrane becomes hyperpolarized, due to the charge inside the membrane becoming more negative.
7.This change in the cell's membrane potential causes voltage-gated calcium channels to close. This leads to a decrease in the influx of calcium ions into the cell and thus the intracellular calcium ion concentration falls.
8.A decrease in the intracellular calcium concentration means that less glutamate is released via calcium-induced exocytosis to the bipolar cell (see below). (The decreased calcium level slows the release of the neurotransmitter glutamate, which can either excite or inhibit the postsynaptic bipolar cells.)
9.Reduction in the release of glutamate means one population of bipolar cells will be depolarized and a separate population of bipolar cells will be hyperpolarized, depending on the nature of receptors (ionotropic or metabotropic) in the postsynaptic terminal (see receptive field).


The eyespot  apparatus/flagella are interdependent 

Eyespots are the simplest and most common "eyes" found in nature, composed of photoreceptors and areas of bright orange-red pigment granules.
Euglena possess a red eyespot, an organelle composed of carotenoid pigment granules. The red spot itself is not thought to be photosensitive. Rather, it filters the sunlight that falls on a light-detecting structure at the base of the flagellum (a swelling, known as the paraflagellar body), allowing only certain wavelengths of light to reach it. As the cell rotates with respect to the light source, the eyespot partially blocks the source, permitting the Euglena to find the light and move toward it (a process known as phototaxis
Phototaxis is a kind of taxis, or locomotory movement, that occurs when a whole organism moves towards or away from stimulus of light.[1] This is advantageous for phototrophic organisms as they can orient themselves most efficiently to receive light for photosynthesis. Phototaxis is called positive if the movement is in the direction of increasing light intensity and negative if the direction is opposite.
so their light sensitiveness has actually nothing to do with seeing. It has a entirely different purpose, namely moves towards or away from stimulus of light . It does not need a brain for doing so.

In order to function, the euglena needs a red eyespot, and a phototaxis receptor. Thats already a interdependent and irreducible complex system system.

the photoreceptors in euglena have the goal to trigger movement in the flagella in order the bacterias to move closer to the light source for photsynthesis. Several parts in the cell are required to accomplish this task, namely : Excitation of this receptor protein results in the formation of cyclic adenosine monophosphate (cAMP) as a second messenger. Chemical signal transduction ultimately triggers changes in flagellar beat patterns and cell movement. No messenger, no movement, no task accomplished...

At its simplest, the eye incorporates three functions:

Light detection
Shading, in the form of dark pigment, for sensing the direction light is coming from
Connection to motor structures, for movement in response to light

Euglena need 

1. a eye spot, 
2. receptor proteins, and their exitations results in cyclic adenosine monophosphate (cAMP) . that will result in beat patterns of
3. the flagella for cell movement. That IS already a irreducible/interdependent complex system.

In some organisms, all three of these functions are carried out by just one cell—the single-celled euglena is one example. It has a light-sensitive spot, pigment granules for shading, and motor cilia. This structure, however, isn't considered a true eye.
The most-basic structure that is widely accepted as an eye has just two cells: a photoreceptor that detects light, and a pigment cell that provides shading. The photoreceptor connects to ciliated cells, which engage to move the animal in response to light. The marine ragworm embryo (right) has a two-celled eye.
if they are not there all at once right from the beginning, even the simplest eye will not work. That is already a irreducible complex system.

Photoreception is a dominant sensory tool found in the majority of taxa across the Metazoa. Photoreceptive organs range in complexity from a single photoreceptor cell, pigmented eyespots and cups, to complicated organs that focus, reflect and absorb light in order to resolve images. Very little is known about how these structures develop and how a simple photoreceptive organ can evolve and elaborate into a more complicated form. 6

96% of animal species have eyes.
http://learn.genetics.utah.edu/content/selection/eye/

Despite much progress, we are at the early stages of fully describing the organization of the human visual system, and we know little about the visual systems of apes.

How did evolution “know” that two eyes were required for 3D vision, or that there was 3D vision in the first place?

In order to take any advantage of improved visual acuity within the eye, the brain must also change in such a way that it is able to interpret the information the eye is sending it.  Otherwise, if the brain is still step up to appreciate only differences in light from dark sent from the eye, without being able to interpret specific patterns of light and dark on the retina, there would be no selective advantage from a dimpled vs. a flat eyespot for example  Because of this requirement, whatever evolution happens to take place in the eye, must be backed up by equivalent evolution in brain development and interpretive powers.

The main optical components of the eye are as follows. First comes the cornea, the transparent, slightly convex outer surface at the centre of the eye. The cornea does not have any blood vessels, so its takes its nutrients from the fluid behind it, known as the aqueous humour, as well as from the fluid in front of it, the tears, which are spread across your cornea when you blink your eyelid.

Next comes the pupil, the opening that lets light enter the eye and ultimately reach the retina. The pupil appears black because of the layer of black pigmented cells that line the back of the eye and absorb the light.

The diameter of the pupil is controlled by the iris, a circular muscle whose pigmentation gives the eye its colour and whose contraction lets the eye adapt continuously to changing light conditions. On a dark night, your pupils are big and black, because your irises open wide to let in as much as possible of the little light available. This reaction is called the pupillary reflex. You can observe it easily yourself, by watching your eyes in a mirror while you turn a nearby light on and off.

After passing through the pupil, the light goes on through the lens, which is suspended between the aqueous humour and the vitreous humour, the fluid that fills the inside of the eye.

The lens in turn focuses the light rays onto the retina, lining the back of the eye. The retina converts the image formed by the light rays into nerve impulses. The optic nerve, composed of the axons of the retina's ganglion cells, then transmits these impulses from the eye to the first visual relay in the brain.



cornea
aqueous humour
pupil
retina
iris
vitreous humour
ganglion cells
conjunctive
cilary muscles
muscle
ocular vein
sclera
choroid
central retina artery
optic nerve sheath
central retinal vein


http://samedical.blogspot.com.br/2010/08/nervous-system-eye.html



Axons which form the optic nerve
Crossed fibers
Uncrossed fibers
optic tract
commissure of gudden
Pulvinar
Lateral geniculate body
superior colliculus
medial geniculate body
nucleus of oculomotor nerve
nucleus of trochlar nerve
nucleus of abducent nerve
striate cortex
Optic radiation


Axons
An axon is a long, branching cell structure that is unique to nerve cells. Like all animal cells, nerve cells — also known as neurons — are covered with a semi-permeable membrane, and it is this membrane that makes up the axons. Axons are responsible for carrying information from the nerve cells to all the other cells of the body. Interference with signals as they travel through the axons has been identified as a cause of certain degenerative neurological disorders.
The neuron itself is composed of three basic structures: the cell body, the axon, and numerous branching dendrites. The cell body houses the nucleus and other organelles. The dendrites collect information from other parts of the body and carry it into the neuron. The axon carries electrical impulses from the neuron to all the other cells of the body. A fatty sheath that covers the structure for the entirety of its length serves to insulate the electrical signals from interference. Known as the myelin sheath, this protective covering is composed primarily of fat cells, and is responsible for the characteristic whitish color of neural tissue.

Optic nerve
The optic nerve, also known as cranial nerve II, transmits visual information from the retina to the brain. 1,2 million neurons  make up the optic nerve, where  incredibly complex electro-chemical codes are formed. These electro-chemical codes are transported to the thalamus of the brain via the optic nerve.

Click on the lower left arrow to see how evolutionists think eyes evolved. Notice how the optic nerve, the immensely complex visual code, and visual cortex are ignored as part of the evolutionary sequence. They are just there in the video, but not even mentioned.
The mixed fibers from the two nerves are continued in the optic tracts, the primary visual centers of the brain. From its mode of development, and from its structure, the optic nerve must be regarded as a prolongation of the brain substance, rather than as an ordinary cerebrospinal nerve.
The optic nerve is a thick bundle of about 1.2 million individual nerve fibers. It travels from the retina to the brain’s vision center, carrying electrical data that the brain will interpret as images.
The individual fibers come from the retina’s photosensitive cells – the rods and cones. Please see our page on The Retina for more information. These cells receive the light that travels into the eye through the cornea, the pupil, the lens and then the vitreous gel. They convert the light data to electrical data so that the nerve fibers can pick it up.

The optic nerve fibers travel across the retina and converge near its center. Their convergence forms the optic nerve. At this location there are no light-sensitive cells, since the nerve fibers are taking up the space. This is the eye’s blind spot. It is near the macula, the retinal area giving us our sharpest, bright-light vision. We use it for reading or any close work where small details are important.

Crossed fibers
The crossed fibers of the optic nerve tend to occupy the medial side of the nerve and the uncrossed fibers the lateral side. In the optic tract, however, the fibers are much more intermingled.

Pulvinar
To effectively interact with our environment, body movements must be coordinated with the perception of visual movement. We will present evidence that regions of the pulvinar nucleus that receive input from the superior colliculus (tectum) may be involved in this process.

Lateral geniculate body
The lateral geniculate nucleus (LGN) is the primary relay center for visual information received from the retina of the eye.The functions of the LGN are multiple. Its unique folding contributes to its utility by performing a range of anatomical calculations without requiring mathematical computations. These include both temporal correlations/decorrelations as well as spatial correlations. The resulting outputs include time correlated and spatially correlated signals resulting from summing the signals received from the left and right semifields of view captured by each of the two eyes. These signals are correlated in order to achieve a three-dimensional representation of object space as well as obtain information for controlling the precision (previously auxiliary) optical system (POS) of the visual modality.
The distribution of the LGN's neurons into various layers suggests that some distinct aspects of the visual information from the retina may be processed separately in this synaptic relay. And that is exactly what has been demonstrated experimentally.

http://thebrain.mcgill.ca/flash/i/i_02/i_02_cr/i_02_cr_vis/i_02_cr_vis.html

superior colliculus
The general function of the tectal system is to direct behavioral responses toward specific points in egocentric ("body-centered") space. Each layer of the tectum contains a topographic map of the surrounding world in retinotopic coordinates, and activation of neurons at a particular point in the map evokes a response directed toward the corresponding point in space.


pretectum
The pretectal area, or pretectum, is a midbrain structure composed of seven nuclei and comprises part of the subcortical visual system. Through reciprocal bilateral projections from the retina, it is involved primarily in mediating behavioral responses to acute changes in ambient light such as the pupillary light reflex, the optokinetic reflex, and temporary changes to the circadian rhythm.

superior colliculus
The superior colliculus is a set of two bumps on the dorsal side of the midbrain. A larger region, the optic tectum, is formed by this structure and the inferior colliculus. Sometimes, the superior colliculus is referred to simply as the tectum. Unlike the inferior colliculus, which is involved in hearing, the tectum plays a role in processing vision.
This structure is involved with visual reflexes. Both the visual cortex and the retina of the eye itself project information to the outer layers of the tectum. Intermediate layers also receive sensory input from both visual and auditory neurons, as well as input from motor centers. The deepest layers receive mainly motor input, and can even direct eye movement and other motor actions. This wide variety of input types helps this structure to move the head and eyes toward sensory stimuli.
In each layer, neurons of the superior colliculus are arranged in a map. This representational map is aligned with retinal cells. Functionally, this allows activation of different retinal cells, triggering a corresponding response on the map. The tectum can then orient the eyes and head in the same direction the stimuli appeared.

Thalamocortical radiations
The optic radiation (also known as the geniculo-calcarine tract or as the geniculostriate pathway or recently posterior thalamic radiation) is a collection of axons from relay neurons in the lateral geniculate nucleus of the thalamus carrying visual information through two divisions (called Upper and Lower division) to the visual cortex (also called striate cortex) along the calcarine fissure.

Striate or visual cortex
The visual cortex of the brain is the part of the cerebral cortex responsible for processing visual information. It is located in the occipital lobe, in the back of the brain.
All visual information that the human mind receives is processed by a part of the brain known as visual cortex. The visual cortex is part of the outermost layer of the brain, the cortex, and is located at the dorsal pole of the occipital lobe; more simply put, at the lower rear of the brain. The visual cortex obtains its information via projections that extend all the way through the brain from the eyeballs. The projections first pass through a stopover point in the middle of the brain, an almond-like lump known as the Lateral Geniculate Nucleus, or LGN. From there they are projected to the visual cortex for processing.





The Purpose of Our Eyes' Strange Wiring Is Unveiled
http://www.scientificamerican.com/article/the-purpose-of-our-eyes-strange-wiring-is-unveiled/
These results mean that the retina of the eye has been optimised so that the sizes and densities of glial cells match the colours to which the eye is sensitive (which is in itself an optimisation process suited to our needs). This optimisation is such that colour vision during the day is enhanced, while night-time vision suffers very little. The effect also works best when the pupils are contracted at high illumination, further adding to the clarity of our colour vision.

Retinal Glial Cells Enhance Human Vision Acuity

http://journals.aps.org/prl/abstract/10.1103/PhysRevLett.104.158102

Abstract
We construct a light-guiding model of the retina outside the fovea, in which an array of glial (Muller) cells permeates the depth of the retina down to the photoreceptors. Based on measured refractive indices, we propagate light to obtain a significant increase of the intensity at the photoreceptors. For pupils up to 6 mm width, the coupling between neighboring cells is only a few percent. Low cross talk over the whole visible spectrum also explains the insensitivity to chromatic aberrations of the eye. The retina is revealed as an optimal structure designed for improving the sharpness of images.

Mystery of the reverse-wired eyeball solved
http://medicalxpress.com/news/2015-02-mystery-reverse-wired-eyeball.html
From a practical standpoint, the wiring of the human eye  doesn't make a lot of sense. In vertebrates, photoreceptors are located behind the neurons in the back of the eye - resulting in light scattering by the nervous fibers and blurring of our vision. Recently, researchers at the Technion - Israel Institute of Technology have confirmed the biological purpose for this seemingly counterintuitive setup. "The retina is not just the simple detector and neural image processor, as believed until today," said Erez Ribak, a professor at the Technion - Israel Institute of Technology. "Its optical structure is optimized for our vision purposes." Ribak and his co-authors will describe their work during the 2015 American Physical Society March Meeting, on Thursday, March 5 in San Antonio, Texas. Ribak's interest in the optical structure of the retina stems from his previous work applying astrophysics and astronomy techniques to improve the ability of scientists and ophthalmologists to view the retina at high detail. Previous experiments with mice had suggested that Müller glia cells, a type of metabolic cell that crosses the retina, play an essential role in guiding and focusing light scattered throughout the retina. To test this, Ribak and his colleagues ran computer simulations and in-vitro experiments in a mouse model to determine whether colors would be concentrated in these metabolic cells. They then used confocal microscopy to produce three-dimensional views of the retinal tissue, and found that the cells were indeed concentrating light into the photoreceptors."For the first time, we've explained why the retina is built backwards, with the neurons in front of the photoreceptors, rather than behind them," Ribak said. Future research for Ribak and his colleagues includes using water-filled goggles to reduce corneal aberrations, allowing observers to gain a finer view of the retina at depth.

Alleged dysteleology of the human eye—the ‘backwards’—vascularized retina
http://creation.com/evolutions-witness-how-eyes-evolved-review
The blind spot, which poses no problems whatsoever for human vision.
One common argument against an Intelligent Designer is the one about the ‘mistake’ of the retinal blood vessels situated above the surface of the retina, ‘obstructing’ the incoming light, as well as the existence of the blind spot. This argument, even on its own terms, has no merit.

Although Schwab does not address this issue in terms of ‘bad’ design, he does provide extensive detail on the vascularization of retinas in the Animal Kingdom and includes a very helpful diagram (p. 250) for comparing and contrasting the different forms of vascularization. The fact that so many different designs of vascular systems exist in the Animal Kingdom demonstrates, if nothing else, that there is no ‘right’ or ‘wrong’ way to construct such a system. Consequently, theological issues aside, it is meaningless to begin even to speak of the vascular system, in the human eye, as a form of bad design. Finally, as elaborated in the next section, whatever the anatomical and physiological limitations of the human eye, they are compensated by the extensive interpretive powers of the human brain.

If a change in selective pressures favored a dimpled eyespot with a slight increase in visual acuity, pretty soon the majority of the population would have dimpled eyespots.  The problem with this notion is that no population of creatures with flat eyespots shows any sort of intra-population range like this were even a small portion of the population has dimpled eyespots to any selectable degree.  This is a common assertion, but it just isn't true.
Now, if these 1,829 gradations really evolutionary steps that are in fact small enough to cross in fairly short order (a few generations each under selective conditions), it seems quite likely that such ranges in morphologic expression would be seen within a single gene pool of a single species.  But, they aren't.  Species that have simple flat light-sensitive eyespots only have flat light-sensitive eyespots.  No individual within that species shows any sort of dimpled eye that would have any selective advantage with regard to increased visual acuity.  This fact alone suggests that these seemingly small steps probably aren't that simple when it comes to the coordinated underlying genetic changes that would be needed to get from one step to the next.

A big problem with these morphologic steps is that they do not take into consideration the fact that vision is more involved than what goes on just within the eye.  In order to take any advantage of improved visual acuity within the eye, the brain must also change in such a way that it is able to interpret the information the eye is sending it.  Otherwise, if the brain is still step up to appreciate only differences in light from dark sent from the eye, without being able to interpret specific patterns of light and dark on the retina, there would be no selective advantage from a dimpled vs. a flat eyespot.  Because of this requirement, whatever evolution happens to take place in the eye, must be backed up by equivalent evolution in brain development and interpretive powers.  

Another interesting problem with the argument for a selective advantage for a dimpled eye over a flat eyespot is the fact that determining the general direction of a light source can be achieved with a flat eyespot.  Dimpling is not needed to determine the relative direction from which a beam of light is coming.  All that is needed is an ability to rotate the eyespot relative to the source of light combined with the brain's ability to associate differences in the intensity of light with the change in orientation of the eyespot relative to the source of light.  This sort of associative ability could produce essentially the same effect of being able to localize and even follow or move toward a source of light without the need for producing a dimpled or cup-shaped eye.  In fact, the species Euglena, with just a flat patch of light-sensitive cells, can swim toward a source of light - - no dimpling needed ( Link ).  In fact, some creatures, like starfish and sea urchin have no eyespots at all yet are still sensitive to light to the degree that they can move toward sources of greater light intensity

1) http://evillusion.wordpress.com/sight-and-sound-a-daunting-task-for-evolution/
2) http://www.reviewevolution.com/press/pressRelease_EyeEvolution.php
3) http://www.grisda.org/origins/21039.htm
4) http://www.detectingdesign.com/humaneye.html
5) http://www.detectingdesign.com/humaneye.html
6) http://www.sicb.org/meetings/2016/schedule/abstractdetails.php?id=1275

The Evolution Of The Visual System In Primates
http://redwood.berkeley.edu/bruno/animal-eyes/Kaas_revised_2013.pdf

http://darwins-god.blogspot.com.br/search?q=eye
Charles Darwin considered the eye to be an “organ of extreme perfection.



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2 The eyespot apparatus is irreducibly complex on Fri Apr 11, 2014 3:37 pm

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http://learn.genetics.utah.edu/content/selection/eye/

Eyes most likely evolved from simple to complex through a gradual series of tiny steps. Piecing together the sequence of eye evolution is challenging, and we don't know the sequence of steps that led to every modern eye. ( despite of this, it evolved. Nice evolution of the gap argument ! )

Light Detection, Pigment, and Movement Make an Eye



Photoreceptor cells

http://en.wikipedia.org/wiki/Photoreceptor_cell



A photoreceptor cell is a specialized type of neuron found in the retina that is capable of phototransduction. The great biological importance of photoreceptors is that they convert light (visible electromagnetic radiation) into signals that can stimulate biological processes. To be more specific, photoreceptor proteins in the cell absorb photons, triggering a change in the cell's membrane potential.



Neuron :

Signal transduction pathway

http://www.youtube.com/watch?v=qOVkedxDqQo

The absorption of light leads to a isomeric change in the retinal molecule.

The signal transduction pathway is the mechanism by which the energy of a photon signals a mechanism in the cell that leads to its electrical polarization. This polarization ultimately leads to either the transmittance or inhibition of a neural signal that will be fed to the brain via the optic nerve. 
The pathway must go through nine highly specific steps, of which any one has no function, unless the whole pathway is been go through. 

Pitman writes : 
The question now of course is, how could such a system evolve gradually?  All the pieces must be in place simultaneously.  For example, what good would it be for euglena that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or "spot" of cells on its head?  These cells now have the ability to detect photons, but so what?  What benefit is that for euglena?  Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them.  So what?!  What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to activate its flagella to swim closer to the light source, or more far away ?   Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the euglena's eyespot.  So what?!  How is euglena going to know what to do with this signal?  It will have to learn what this signal means.  Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems.  Now euglena, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring.  If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them.  All of these wonderful processes need regulation.  No function is beneficial unless it can be regulated (turned off and on).  If the light sensitive cells cannot be turned off once they are turned on, vision does not occur.  This regulatory ability is also very complicated involving a great many proteins and other molecules - all of which must be in place initially for vision to be beneficial.


The steps, or signal transduction pathway, in the vertebrate eye's rod and cone photoreceptors are then:

1.The rhodopsin or iodopsin in the disc membrane of the outer segment absorbs a photon, changing the configuration of a retinal Schiff base cofactor inside the protein from the cis-form to the trans-form, causing the retinal to change shape.

2.This results in a series of unstable intermediates, the last of which binds stronger to the G protein in the membrane and activates transducin, a protein inside the cell. This is the first amplification step – each photoactivated rhodopsin triggers activation of about 100 transducins. (The shape change in the opsin activates a G protein called transducin.)

3.Each transducin then activates the enzyme cGMP-specific phosphodiesterase (PDE).

4.PDE then catalyzes the hydrolysis of cGMP to 5' GMP. This is the second amplification step, where a single PDE hydrolyses about 1000 cGMP molecules.

5.The net concentration of intracellular cGMP is reduced (due to its conversion to 5' GMP via PDE), resulting in the closure of cyclic nucleotide-gated Na+ ion channels located in the photoreceptor outer segment membrane.

6.As a result, sodium ions can no longer enter the cell, and the photoreceptor outer segment membrane becomes hyperpolarized, due to the charge inside the membrane becoming more negative.

7.This change in the cell's membrane potential causes voltage-gated calcium channels to close. This leads to a decrease in the influx of calcium ions into the cell and thus the intracellular calcium ion concentration falls.

8.A decrease in the intracellular calcium concentration means that less glutamate is released via calcium-induced exocytosis to the bipolar cell (see below). (The decreased calcium level slows the release of the neurotransmitter glutamate, which can either excite or inhibit the postsynaptic bipolar cells.)

9.Reduction in the release of glutamate means one population of bipolar cells will be depolarized and a separate population of bipolar cells will be hyperpolarized, depending on the nature of receptors (ionotropic or metabotropic) in the postsynaptic terminal (see receptive field).

Thus, a rod or cone photoreceptor actually releases less neurotransmitter when stimulated by light. Less neurotransmitter could either stimulate (depolarize) or inhibit (hyperpolarize) the bi-polar cell it synapses with, dependent on the nature of the receptor on the bipolar cell. This ability is integral to the center on/off mapping of visual units.[citation needed]

ATP provided by the inner segment powers the sodium-potassium pump. This pump is necessary to reset the initial state of the outer segment by taking the sodium ions that are entering the cell and pumping them back out.

Although photoreceptors are neurons, they do not conduct action potentials with the exception of the photosensitive ganglion cell – which are involved mainly in the regulation of circadian rhythms, melatonin, and pupil dilation.


Advantages


Phototransduction in rods and cones is unique in that the stimulus (in this case, light) actually reduces the cell's response or firing rate, which is unusual for a sensory system where the stimulus usually increases the cell's response or firing rate. However, this system offers several key advantages.

First, the classic (rod or cone) photoreceptor is depolarized in the dark, which means many sodium ions are flowing into the cell. Thus, the random opening or closing of sodium channels will not affect the membrane potential of the cell; only the closing of a large number of channels, through absorption of a photon, will affect it and signal that light is in the visual field. Hence, the system is noiseless.

Second, there is a lot of amplification in two stages of classic phototransduction: one pigment will activate many molecules of transducin, and one PDE will cleave many cGMPs. This amplification means that even the absorption of one photon will affect membrane potential and signal to the brain that light is in the visual field. This is the main feature that differentiates rod photoreceptors from cone photoreceptors. Rods are extremely sensitive and have the capacity of registering a single photon of light, unlike cones. On the other hand, cones are known to have very fast kinetics in terms of rate of amplification of phototransduction, unlike rods.

http://www.detectingdesign.com/humaneye.html

the first step in vision is the detection of photons.  In order to detect a photon, specialized cells use a molecule called 11-cis-retinal.  When a photon of light interacts with this molecule, it changes its shape almost instantly.  It is now called trans-retinal.  This change in shape causes a change in shape of another molecule called rhodopsin.  The new shape of rhodopsin is called metarhodopsin II.  Metarhodopsin II now sticks to another protein called transducin forcing it to drop an attached molecule called GDP and pick up another molecule called GTP.  The GTP-transducin-metarhodopsin II molecule now attaches to another protein called phosphodiesterase.  When this happens, phosphodiesterase cleaves molecules called cGMPs.  This cleavage of cGMPs reduces their relative numbers in the cell.  This reduction in cGMP is sensed by an ion channel.  This ion channel shuts off the ability of the sodium ion to enter the cell.  This blockage of sodium entrance into the cell causes an imbalance of charge across the cell's membrane.  This imbalance of charge sends an electrical current to the brain.  The brain then interprets this signal and the result is called vision.

11-cis-retinal
rhodopsin ==>> becomes metarhodopsin II + transducin  , drops GDP + adds GTP

GTP-transducin-metarhodopsin II + phosphodiesterase

phosphodiesterase cleaves cGMPs == >> blockage of sodium entrance into the cell

imbalance of charge across the cell's membrane.  This imbalance of charge sends an electrical current to the brain.  The brain then interprets this signal and the result is called vision.

Many other proteins are now needed to convert the proteins and other molecules just mentioned back to their original forms so that they can detect another photon of light and signal the brain.  If any one of these proteins or molecules is missing, even in the simplest eye system, vision will not occur

The question now of course is, how could such a system evolve gradually?  All the pieces must be in place simultaneously.  For example, what good would it be for an earthworm that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or "spot" of cells on its head?  These cells now have the ability to detect photons, but so what?  What benefit is that to the earthworm?  Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them.  So what?!  What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to the worm's minute brain?   Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the worm's brain.  So what?!  How is the worm going to know what to do with this signal?  It will have to learn what this signal means.  Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems.  Now the earthworm, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring.  If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them.  All of these wonderful processes need regulation.  No function is beneficial unless it can be regulated (turned off and on).  If the light sensitive cells cannot be turned off once they are turned on, vision does not occur.  This regulatory ability is also very complicated involving a great many proteins and other molecules - all of which must be in place initially for vision to be beneficial.

Arguments against IC of the signal transduction pathway

http://www.asa3.org/evolution/irred_compl.html

Second, concerning vision. The argument has been made that the vision system is also an irreducibly complex system. Mike Behe has found no fault in Darwin's lack of concern with the origin of light reception at the detailed cellular and molecular level, but now with our opening of the black box of vision, we have no excuse for not concerning ourselves with those sort of details. Mike claims that upon examination of the open box that we must conclude that evolution of this complex system is impossible. So again we must ask, does the pre-adaptation argument get us anywhere in the discussion of the origin of vision? Again, the answer is an obvious yes. First, if we restrict ourselves to light reception, then I think that it's fair to say that a nerve cell is a pre adaptation to vision. Given a nerve cell, I don't have to explain where all those components come from (at least when explaining vision). Second, transducin, one of the key proteins involved in the light signal transduction from rhodopsin to nerve cell, is a member of the G protein family, a large family involved in all sorts of signal transduction events, including hormone signaling. The main novel feature of transducin is its specificity for rhodopsin. The generic G protein is a pre adaptation for transducin. Finally, rhodopsin, the main light reception protein, is a membrane protein similar in structure to other sensory receptors and to hormone receptors. These other receptors whose physiological effects are also mediated by G proteins may have been pre adaptations for rhodopsin. My answer here may be a form of question-begging, because you can always ask where did these other systems come from, but I think that the functional diversification of similar signal transduction sytems is reminiscent of the hemoglobin tale told above. What's needed is detailed sequence and structure information about all these proteins in a variety of organisms that are representative of the tree of life. Then maybe we can say that we have opened the black box. Until then, I think that given the present data that the evolutionary explanation for complexity is not only plausible but likely.
This answer does not address the key issue of IC, namely that unless the process goes all steps through, no function is achieved.



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http://www.csa.com/discoveryguides/sensory/review2.php

Our senses do not work in isolation. An eye is useless without a brain that can interpret its input correctly. Furthermore, the brain cannot make sense of the eye without any other sensory input. Research shows our eyes must perform saccades to continually refresh the image, and the brain must also track where the head is and how it is moving. Other muscles also control the shape and length of the lens to allow proper focusing. All this requires feedback from our proprioception—our knowledge of where our body is and what it is doing in space—and the vestibular system, which controls our sense of balance. Disrupting the vestibular system by squirting fluid in the ear or by spinning the person will cause nystagmus—rapid involuntary back and forth movement of the eyes, which ruins vision's efficiency; they cannot focus to read, judge distance and so on until the nystagmus stops. This inner chaos also affects people's ability to focus on what others are saying, as well. This intense interdependence between balance, self-movement, and vision is why artificial eyes are a long way away from becoming a viable option. A fully functional artificial eye would need to be correctly attached to and controlled by eye muscles and the optic nerve itself—a very complex, virtually impossible feat of surgery and healing in a very sensitive part of the head. This is also why whole eye transplants cannot be done, just corneal transplants and other forms of eye surgery.

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http://www.wikihow.com/Argue-Against-Evolution-of-Eyesight

eye / brain is a interdependent and irreducible complex system

What would you think of a person who saw a computer chip with millions of transistors that were self-connected into a computer and it all worked--who said,

"You know that spontaneous events formed that computer chip by electrical and mineral activity -- multiprocessing program included? It is scientific fact that the chip obviously had no designer, no plan or maker! Oh, that is explained by billions of years of processes by pressures of nature..."

You would think that person was not just confused. Yet, the evolutionist essentially says that's how the optic center in the brain came to exist, and that is a more interdependent processor than the most advanced computer chip ever made. So they say that the optic nerves, the eye and the retina all happened by a series of natural events that we can call ad hoc mistake--"formed in one particular moment without ability to consider any application."

So then is the existence of a gnat or mosquito, with exquisite processing that enables flight, formed without logic, design or awareness, in that process... need it be so. Evolutionists may even propose that it was not by random chaos. How would evolution not be "random chaos?" That's a fair question to ask.

Evolutionists argue that [non-directed] features that improve a creature’s chance for survival get passed on in succeeding generations. Is it just as logical that all mutations would be passed on? Whether or not they are beneficial there is no awareness of the process by the genetic system. So, how would the unrelated parts of an eye and a brain now correlate, by independent mutations--all "failures" of the previously existing genetic process. Unobservant processes that did not realize their own existence then continued, added, subtracted by failures (mutations) of the genetic system, and perhaps surviving to breed, and therefore passing on defects, or dying before they get a chance to breed!

How the Body Works: Overview of the Nervous and Endocrine Systems

http://drbenkim.com/nervous-endocrine-system.htm

The interdependent relationship between your nervous and endocrine systems begins in a tiny area of tissue in your brain called your hypothalamus.

Your hypothalamus is only about as large as a grape, and can be viewed as the micro-processing chip that controls almost all of your body's external and internal activities. Your hypothalamus receives information from all of the major areas of your brain, your major organs, and your eyes, and it registers sensations like pain, temperature, hunger, thirst, lust, stress, fear, and anger.

Once your hypothalamus registers incoming information and decides what your body needs to best survive and be healthy, it uses your autonomic nervous system to affect the behavior of all of your major organs. Examples of such effects are increased heart and lung rates, increased blood flow to your skeletal muscles or digestive organs, changes in how much light enters your eyes and how well your eyes can focus on distant objects, production of sweat or shivers, and arousal of sexual organs.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246854/

biochemists have shown that even a simple light-sensitive spot requires a complex array of enzyme systems. When light strikes the retina, a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. The change in the shape of the retinal molecule forces a change in the shape of the protein rhodopsin. The protein then changes to metarhodopsin II and sticks to another protein, called transducin. This process requires energy in the form of GTP, which binds to transducin. GTP-transducin-metarhodopsin II then binds to a protein called phosphodiesterase, located on the cell wall. This affects the cGMP levels within the cell, leading to a signal that then goes to the brain. The recognition of this signal in the brain and subsequent interpretation involve numerous other proteins and enzymes and biochemical reactions within the brain cells. Thus, each of these enzymes and proteins must exist for the system to work properly. Many other mathematical and logistical weaknesses to the Nilsson example of eye evolution have been uncovered (28). In summary, the eye is incredibly complex. Since it is unreasonable to expect self-formation of the enzymes in perfect proportion simultaneously, eye function represents a system that could not have arisen by gradual mutations.

http://genesisfile.com/?page_id=146

Complexity of the Eye and Brain

Without the foresight of a plan, we would expect that the random evolutionary changes would attempt all kinds of useless combinations of parts while trying to provide for a successful evolutionary advancement. Yet as we look at living organisms over the world, we do not seem to see any of these random combinations. In nature, it appears that we are dealing largely, if not exclusively, with purposeful parts. Furthermore, if evolution is a real ongoing process, why don’t we find new developing complex organs in organisms that lack them? We would expect to find developing legs, eyes, livers, and new unknown kinds of organs, providing for evolutionary advancement in organisms that lacked desirable advantages. This absence is a serious indictment against any proposed undirected evolutionary process, and favors the concept that what we see represents the work of an intelligent Creator.

The simple example of a muscle, mentioned above, pales into insignificance when we consider more complicated organs such as the eye or the brain. These contain many interdependent systems composed of parts that would be useless without the presence of all the other necessary parts. In these systems, nothing works until all the necessary components are present and working. The eye has an automatic focusing system that adjusts the lens so as to permit us to clearly see close and distant objects. We do not fully understand how it works, but a part of the brain analyzes data from the eye and controls the muscles in the eye that change the shape of the lens. The system that controls the size of the pupil so as to adjust to light intensity and to reduce spherical lens aberration also illustrates interdependent parts. Then there are the 100,000,000 light-sensitive cells in the human eye that send information to the brain through some 1,000,000 nerve fibers of the optic nerve. In the brain this information is sorted into various components such as color, movement, form and depth. It is then analyzed and combined into an intelligible picture. This involves an extremely complex array of interdependent parts.

But the visual process is only part of our complex brains, which contain some 100,000,000,000 nerve cells connected by some 400,000 kilometers of nerve fibres. It is estimated that there are around 100,000,000,000,000 connections between nerve cells in the human brain. That we can think straight (we hope most of us do!) is a witness to a marvelous ordered complex of interdependent parts that challenges suggestions of an origin by random evolutionary changes. How could such complicated organs develop by an unplanned process?

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http://www.brainfacts.org/sensing-thinking-behaving/senses-and-perception/articles/2012/vision-it-all-starts-with-light/

For the brain to process visual information, light waves must first pass through the eyes. The sensitive photoreceptors of the retina then transmits the electrochemical feeds from the eye to the brain. The visual centers of the brain then process and decode the transmitted signals, which is now perceived as visual information.

Both your eyes and your brain have a role in vision; it isn't a task that a single organ does.
Your eyes collect light and turn it into electrical signals. Your brain then processes those signals and converts it to an image that you can understand.
The eyes do not see anything. Light impinges on photo-receptors in the retina (which, technically, is part of the brain, but I won't be considering it as such) and nerve impulses are generated by RGCs and sent to the brain via the optic nerve. You do not perceive images until signal processing occurs in the brain (visual cortex and related visual areas). So there is a interdependence. Without the eye, you don't see. Without the brain, you don't see either. Both are required.


http://www.compellingtruth.org/irreducible-complexity.html

The eye: Although evolutionists have attempted to show how the eye could have evolved, the sheer complexity of the mechanism defies explanation. The retina actually interprets much of the input before it reaches the brain. The processors in the brain would have had to evolve parallel with yet independently of the development of the eye itself. Even the computer simulation of the evolution of the eye shows how only an intentional design could have resulted in such functionality.


http://www.wikihow.com/Argue-Against-Evolution-of-Eyesight

eye / brain is a interdependent and irreducible complex system

If the sight center of the brain that “sees” did not “begin” to correctly process sight at exactly at the same moment as the optic nerve, then the nerve would have no reason to transmit or to be attached to the brain and the eye wouldn’t see.

What would you think of a person who saw a computer chip with millions of transistors that were self-connected into a computer and it all worked--who said,

"You know that spontaneous events formed that computer chip by electrical and mineral activity -- multiprocessing program included? It is scientific fact that the chip obviously had no designer, no plan or maker! Oh, that is explained by billions of years of processes by pressures of nature..."

You would think that person was not just confused. Yet, the evolutionist essentially says that's how the optic center in the brain came to exist, and that is a more interdependent processor than the most advanced computer chip ever made. So they say that the optic nerves, the eye and the retina all happened by a series of natural events that we can call ad hoc mistake--"formed in one particular moment without ability to consider any application."

So then is the existence of a gnat or mosquito, with exquisite processing that enables flight, formed without logic, design or awareness, in that process... need it be so. Evolutionists may even propose that it was not by random chaos. How would evolution not be "random chaos?" That's a fair question to ask.

Evolutionists argue that [non-directed] features that improve a creature’s chance for survival get passed on in succeeding generations. Is it just as logical that all mutations would be passed on? Whether or not they are beneficial there is no awareness of the process by the genetic system. So, how would the unrelated parts of an eye and a brain now correlate, by independent mutations--all "failures" of the previously existing genetic process. Unobservant processes that did not realize their own existence then continued, added, subtracted by failures (mutations) of the genetic system, and perhaps surviving to breed, and therefore passing on defects, or dying before they get a chance to breed!


How the Body Works: Overview of the Nervous and Endocrine Systems

http://drbenkim.com/nervous-endocrine-system.htm

The interdependent relationship between your nervous and endocrine systems begins in a tiny area of tissue in your brain called your hypothalamus.

Your hypothalamus is only about as large as a grape, and can be viewed as the micro-processing chip that controls almost all of your body's external and internal activities. Your hypothalamus receives information from all of the major areas of your brain, your major organs, and your eyes, and it registers sensations like pain, temperature, hunger, thirst, lust, stress, fear, and anger.

Once your hypothalamus registers incoming information and decides what your body needs to best survive and be healthy, it uses your autonomic nervous system to affect the behavior of all of your major organs. Examples of such effects are increased heart and lung rates, increased blood flow to your skeletal muscles or digestive organs, changes in how much light enters your eyes and how well your eyes can focus on distant objects, production of sweat or shivers, and arousal of sexual organs.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3246854/

biochemists have shown that even a simple light-sensitive spot requires a complex array of enzyme systems. When light strikes the retina, a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. The change in the shape of the retinal molecule forces a change in the shape of the protein rhodopsin. The protein then changes to metarhodopsin II and sticks to another protein, called transducin. This process requires energy in the form of GTP, which binds to transducin. GTP-transducin-metarhodopsin II then binds to a protein called phosphodiesterase, located on the cell wall. This affects the cGMP levels within the cell, leading to a signal that then goes to the brain. The recognition of this signal in the brain and subsequent interpretation involve numerous other proteins and enzymes and biochemical reactions within the brain cells. Thus, each of these enzymes and proteins must exist for the system to work properly. Many other mathematical and logistical weaknesses to the Nilsson example of eye evolution have been uncovered (28). In summary, the eye is incredibly complex. Since it is unreasonable to expect self-formation of the enzymes in perfect proportion simultaneously, eye function represents a system that could not have arisen by gradual mutations.

http://genesisfile.com/?page_id=146

Complexity of the Eye and Brain

Without the foresight of a plan, we would expect that the random evolutionary changes would attempt all kinds of useless combinations of parts while trying to provide for a successful evolutionary advancement. Yet as we look at living organisms over the world, we do not seem to see any of these random combinations. In nature, it appears that we are dealing largely, if not exclusively, with purposeful parts. Furthermore, if evolution is a real ongoing process, why don’t we find new developing complex organs in organisms that lack them? We would expect to find developing legs, eyes, livers, and new unknown kinds of organs, providing for evolutionary advancement in organisms that lacked desirable advantages. This absence is a serious indictment against any proposed undirected evolutionary process, and favors the concept that what we see represents the work of an intelligent Creator.

The simple example of a muscle, mentioned above, pales into insignificance when we consider more complicated organs such as the eye or the brain. These contain many interdependent systems composed of parts that would be useless without the presence of all the other necessary parts. In these systems, nothing works until all the necessary components are present and working. The eye has an automatic focusing system that adjusts the lens so as to permit us to clearly see close and distant objects. We do not fully understand how it works, but a part of the brain analyzes data from the eye and controls the muscles in the eye that change the shape of the lens. The system that controls the size of the pupil so as to adjust to light intensity and to reduce spherical lens aberration also illustrates interdependent parts. Then there are the 100,000,000 light-sensitive cells in the human eye that send information to the brain through some 1,000,000 nerve fibers of the optic nerve. In the brain this information is sorted into various components such as color, movement, form and depth. It is then analyzed and combined into an intelligible picture. This involves an extremely complex array of interdependent parts.

But the visual process is only part of our complex brains, which contain some 100,000,000,000 nerve cells connected by some 400,000 kilometers of nerve fibres. It is estimated that there are around 100,000,000,000,000 connections between nerve cells in the human brain. That we can think straight (we hope most of us do!) is a witness to a marvelous ordered complex of interdependent parts that challenges suggestions of an origin by random evolutionary changes. How could such complicated organs develop by an unplanned process?

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The Nilsson and Pelger Theory of Eye Evolution

http://adarwinstudygroup.org/biology-culture-psychology/design-or-natural-selection/#img-01-1803

Since Darwin's time, our understanding of genetics has opened the door to comprehending what previously seemed impossible. In a 1994 paper, for example, Dan Nilsson and Susanne Pelger produced a dramatic example of computer modeling that illustrated how an eye could evovle in fewer than 400,000 “generations.” Random mutations of the refractive index of the surface membrane were incorporated into the algorithm, along with selective pressure for only 1% improvement each time. A steadily improving lens and eyecup resulted, solving the question asked agonizingly by Darwin, how could a structure as complex as the eye evolve? The answer from this model is: in a geological eyeblink, improved eyes can evolve in which each stage provides a better eye than the last.



http://www.rpgroup.caltech.edu/courses/aph161/Handouts/Nilsson1994.pdf

The evolution of complex structures, however, involves modifications of a large number of separate quantitative characters, and in addition there may be discrete innovations and an unknown number of hidden but necessary phenotypic changes. These complications seem effectively to prevent evolution rate estimates for entire organs and other complex structures. An eye is unique in this respect because the structures necessary for image formation, although there may be several, are all typically quantitative in their nature, and can be treated as local modifications of pre-existing tissues. Taking a patch of pigmented light-sensitive epithelium as the starting point, we avoid the more inaccessible problem of photoreceptor cell evolution. Thus, if the objective is limited to finding the number of generations required for the evolution of an eye’s optical geometry, then the problem becomes solvable.

http://darwins-god.blogspot.com.br/search?q=eye



Evolution Can Even Explain How the Human Eye Evolved

Benjamin Radford writes for the Discovery News and is interested in why people believe things for which there is little or no evidence. He applies critical thinking and scientific methodologies to unusual claims. One of those things that interests Radford is skepticism of evolution. After all, as Radford notes, there is “overwhelming scientific evidence for evolution,” and it is “confirmed by nearly every scientific discipline.” Evolution is all around us, all the time. Evolution is why we need to get a new flu shot every year and, notes Radford, evolution can even explain how the human eye evolved. It is strange that such claims come from a critical thinker such as Radford because, in fact, they are all false.

Consider the evolution of the human eye. Charles Darwin considered the eye to be an “organ of extreme perfection.” Even after writing Origins he confessed it gave him a cold shudder. He needed to focus on his theory’s fine gradations to give himself comfort. But one hundred and thirty four years later, in 1994, evolutionists claimed they had solved the problem. The evolution of the eye was finally understood. It turned out such evolution was no big deal after all. In fact the eye could rather easily evolve.

The only catch to the conclusion was that it was circular. The evolutionists, who believe evolution is a fact, first assumed the evolution of the eye in order to solve the problem of the evolution of the eye.

With evolution taken as a given, whether or not vision systems evolved was no longer in question—they did. The only question was how they have evolved. The 1994 paper explained that although Darwin “anticipated that the eye would become a favorite target for criticism,” the problem “has now almost become a historical curiosity” and “the question is now one of process rate rather than one of principle.” The evolutionists estimated this rate by first assuming that the eye indeed evolved. They wrote:

   The evolution of complex structures, however, involves modifications of a large number of separate quantitative characters, and in addition there may be discrete innovations and an unknown number of hidden but necessary phenotypic changes. These complications seem effectively to prevent evolution rate estimates for entire organs and other complex structures. An eye is unique in this respect because the structures necessary for image formation, although there may be several, are all typically quantitative in their nature, and can be treated as local modifications of pre-existing tissues. Taking a patch of pigmented light-sensitive epithelium as the starting point, we avoid the more inaccessible problem of photoreceptor cell evolution. Thus, if the objective is limited to finding the number of generations required for the evolution of an eye’s optical geometry, then the problem becomes solvable.


The problem becomes solvable? The evolutionists skipped the entire evolution of cellular signal transduction and the vision cascade. That would be like saying you have showed how motorcycles evolved although you took the engine, drive train and wheels as your starting point.

The evolutionists then skipped all of the major problems that arise after you have a signal transduction system in place, such as the incredible post processing system and the creation of the machinery to construct the vision system. The problem they ended up solving is sometimes affectionately referred to as a “cartoon” version of the real world problem.

The research, if you can call it that, did not demonstrate that the eye evolved or could have evolved. Yet the paper became a favorite reference for evolutionists wanting to promote evolution. Eye evolution, they insisted, was now known to be straightforward. Here, for instance, is how our tax dollars are used by PBS to promote this abuse of science:

   Zoologist Dan-Erik Nilsson demonstrates how the complex human eye could have evolved through natural selection acting on small variations. Starting with a simple patch of light sensitive cells, Nilsson’s model “evolves” until a clear image is produced.



This spreading of false information is not limited to popular presentations. A paper reporting on “highly advanced compound eyes” which are “as advanced as those of many living forms” in early arthropods begins by informing the reader that “theory (i.e., the Nilsson paper) suggests that complex eyes can evolve very rapidly.” This helps them to conclude that those incredible arthropod eyes are “further evidence that the Cambrian explosion involved rapid innovation.”

With the mythological framework in place, the findings could then safely be presented as confirmations of evolution. As the journal’s editor added:

   Charles Darwin thought that the eye, which he called an “organ of extreme perfection,” was a serious challenge to evolutionary theory — but he was mistaken. Theory predicts that eyes can evolve with great speed, and now there is support for this prediction from the fossil record.


Support for this prediction? You’ve got to be kidding. A cartoon version of reality, taking the myth of evolution as true, is considered a “prediction” and amazing early complexity in the fossils then becomes a “support for this prediction”?

What the arthropod fossils revealed is an early Cambrian, highly advanced vision system more elaborate than any so far discovered. Its compound eyes have more then 3,000 lenses optimally arranged in the densest and most efficient packing pattern. As the paper explains:

   The extremely regular arrangement of lenses seen here exceeds even that in certain modern taxa, such as the horseshoe crab Limulus, in which up to one-third of lenses deviate from hexagonal packing.


All of this is presented to the reader as merely another demonstration of how fantastic designs just happen spontaneously to arise:

   The new fossils reveal that some of the earliest arthropods had already acquired visual systems similar to those of living forms, underscoring the speed and magnitude of the evolutionary innovation that occurred during the Cambrian explosion.


Ho-hum, yet more evolutionary innovation. For evolutionists it was just another day in the office. As PZ Myers explained, we already knew that complex animals appear rapidly. After all, that is why they call it the “Cambrian explosion.” Evolutionists have written “whole books on the subject.”

Myers follows this circular reasoning with yet more question begging:

The sudden appearance of complexity is no surprise, either. We know that the fundamental mechanisms of eye function evolved long before the Cambrian, from the molecular evidence;



Of course there is no “molecular evidence” that gives us such knowledge (see here for example). But if you assume evolution is true to begin with, as do evolutionists who analyze the molecular patterns, then Myers’ fictional, question begging, world makes sense.

Myers follows these circular arguments with a more subtle type of fallacy. He explains that these particular findings are no big deal because both this finding and the similar trilobite vision systems require cellular signal transduction, development machines and so forth:

   It is also the case that the measure of complexity here is determined by a simple meristic trait, the number of ommatidia. This is not radical. The hard part in the evolution of the compound eye was the development of the signal transduction mechanism, followed by the developmental rules that governed the formation of a regular, repeating structure of the eye. The number of ommatidia is a reflection of the degree of commitment of tissues in the head to eye formation, and is a quantitative difference, not a qualitative one.


Setting aside the usual evolutionary speculation about how easily designs evolve, the problem here is that the cellular signal transduction, development machines and so forth are themselves problems for evolution. Indeed, even the simplest of light detection systems sport such incredible designs for which evolution has no explanation beyond vague speculation.

Next Myers is back to question-begging. In typical fashion he attempts to shore up the evolution position with the usual reference to, yes, the mythical 1994 Nilsson paper:

   And finally, there’s nothing in the data from this paper that implies sudden origins; there can’t be. If it takes a few hundred thousand years for a complex eye to evolve from a simple light sensing organ, there is no way to determine that one sample of a set of fossils was the product of millions of years of evolution, or one day of magical creation.

Next is the fallacy of credulity. If you present an evolutionist with the scientific failures of his theory, he will accuse you of basing your skepticism on your own failure to imagine a solution. As Myers puts it:

It’s a logical error and a failure of the imagination to assume that these descriptions are of a population that spontaneously emerged nearly-instantaneously.

Failure of the imagination? Indeed, we just need to do more imagining, that’s the problem.

Finally Myers reiterates the flawed Darwinian argument that whatever abruptness you see in the fossil record is, after all, merely a consequence of all those gaps in the fossils:

Darwin himself explained in great detail how one should not expect fine-grained fossil series, due to the imperfection of the geological record.


When in doubt, doubt the data. Paleontologists agree that the fossil record reveals abrupt appearances, but when convenient evolutionists can always protect their theory with those gaps in the fossil record.

Evolutionary thinking is remarkable. I am reminded of John Earman’s remarks about Hume’s arguments. For it is astonishing how well evolution is treated, given how completely the confection collapses under a little probing. So if Benjamin Radford really is interested in why people believe things for which there is little or no evidence, we have just the topic for him.

http://musingsofscience.wordpress.com/2011/01/22/evolution-of-the-eye-nilsson-pelger-and-lens-evolution/



http://www.reviewevolution.com/press/pressRelease_EyeEvolution.php

Since Nilsson and Pelger's article was published, it has been widely--but erroneously--reported that their conclusions were based on a computer model. Berlinski calls this claim "an urban myth." At a minimum, PBS should make clear to viewers that Nilsson's conclusions are not based on computer models at all, and it should acknowledge that his work is highly speculative."

http://creationwiki.org/The_eye_is_too_complex_to_have_evolved_%28Talk.Origins%29

http://www.grisda.org/origins/21039.htm

"What is one to make of all this? First, comparing the evolution of the eye to shape changes on a computer screen seems rather far-fetched. The entire project seems closer to an exercise in geometry than in biology. Second, the exercise assumes a functional starting point. Thus it has nothing to do with the origin of the biochemical systems of vision or the requisite neural network. Third, Nilsson and Pelger's computer exercise operates as if each 1% change in morphology can be accounted for by a single gene mutation. They do not consider the effects of pleiotropy, genetic background, or developmental processes. Fourth, an important part of the model relies on the special circumstance of a layer of clear cells covering the "retina." This layer somehow assumes the proper shape of a lens. Fifth, as noted by the authors, several features of the eye remain unaccounted for, such as the iris. Basically, the only result achieved was to show that two light-sensitive surfaces that differ in shape by 1% will have different efficiencies in photoreception, and that an uninterrupted series of 1% improvements is possible. The failure of scientists to produce new structures in selection experiments illustrates the implausibility of Nilsson and Pelger's "just so" story."



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Chance or design?

http://creation.com/excellent-eye-better-than-any-camera-the-eyes-response-to-light

Far from being a poor design, the eye’s dynamic range exceeds that of the best man-made photodetectors. And this latest research shows the intricate microscopic machinery behind it—a motor, glue, ‘calmer’ and internal ‘train tracks’.

All these features would need to be present and coordinated; otherwise, the eye would be blinded by bright light.4 Thus natural selection could not build this system up step-by-step, since each step by itself has no advantage over the previous step, until all steps are complete.

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8 Evolutionists Solve Eye Evolution (Again) on Mon Apr 21, 2014 10:40 pm

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Evolutionists Solve Eye Evolution (Again)

http://darwins-god.blogspot.com.br/2012/11/evolutionists-solve-eye-evolution-again.html

Recently we discussed a paper from 2008 in which evolutionists claimed to have solved the long-standing question of how the eye evolved. It is a problem that famously once made Darwin shudder but the evolutionists claimed that now, with our advanced scientific knowledge, “the gap in understanding of the molecular evolution of eye components is all but closed.” That was quite a claim and, not surprisingly, there was no such breakthrough. In fact, the “explanation” that the evolutionists provided was simply that the key cellular signal transduction pathway in our eyes came from a very similar pathway in yeast that senses certain types of signaling chemicals known as pheromones. The evolutionists had no explanation for how the yeast pathway arose in the first place or exactly how it could morph into the animal vision system. It was yet another example of evolution’s trivial, non scientific, solutions that do nothing but generate vacuous headlines. Well evolutionists have done it again. This month they “solved” the problem of eye evolution yet again. Apparently that 2008 solution didn’t take, but this new solution is no better.

You may have seen the Wall Street Journal article from earlier this month proclaiming the new discovery of how vision evolved. The headline read, “A Relief to Darwin: The Eyes Have It.” Or perhaps you saw the press release trumpeting the new “Breakthrough study” that “Pinpoints Evolutionary Origins of Sight.”

The paper itself was no less triumphant. It claimed to reveal “a simple route to animal vision.” But in fact the evolutionists discovered no such thing. It was all yet another abuse of science.

As with the earlier 2008 paper, the new study appeals to yet another signal transduction pathway as the progenitor of later vision systems. This time instead of yeast, the paper appeals to a pathway in placozoa. As with the yeast system, the placozoa system probably detects signaling chemicals.

As usual, the evolutionists “solve” the problem simply by pushing it back in time. The evolution narrative continues to push complexity to earlier stages where it somehow and fortuitously appears. As the evolutionists conclude: “Our results are compatible with the view that the last common neuralian ancestor might have been more complex than generally assumed.”

So the new study makes evolution even more heroic and implausible. What it does not show is precisely what the paper and the articles claim that it shows: how vision evolved.

Evolution is more ludicrous with each passing week. It is a religiously-motivated movement that force-fits scientific findings to its truth. Its unending trail of vacuous discoveries is nothing more than a reflection of the underlying religion. As John Ioannidis has put it, “claimed research findings may often be simply accurate measures of the prevailing bias.” That is a good description of evolutionary science.

Religion drives science and it matters.


Metazoan opsin evolution reveals a simple route to animal vision


http://www.pnas.org/content/109/46/18868

Abstract

All known visual pigments in Neuralia (Cnidaria, Ctenophora, and Bilateria) are composed of an opsin (a seven-transmembrane G protein-coupled receptor), and a light-sensitive chromophore, generally retinal. Accordingly, opsins play a key role in vision. There is no agreement on the relationships of the neuralian opsin subfamilies, and clarifying their phylogeny is key to elucidating the origin of this protein family and of vision. We used improved methods and data to resolve the opsin phylogeny and explain the evolution of animal vision. We found that the Placozoa have opsins, and that the opsins share a common ancestor with the melatonin receptors. Further to this, we found that all known neuralian opsins can be classified into the same three subfamilies into which the bilaterian opsins are classified: the ciliary (C), rhabdomeric (R), and go-coupled plus retinochrome, retinal G protein-coupled receptor (Go/RGR) opsins. Our results entail a simple scenario of opsin evolution. The first opsin originated from the duplication of the common ancestor of the melatonin and opsin genes in a eumetazoan (Placozoa plus Neuralia) ancestor, and an inference of its amino acid sequence suggests that this protein might not have been light-sensitive. Two more gene duplications in the ancestral neuralian lineage resulted in the origin of the R, C, and Go/RGR opsins. Accordingly, the first animal with at least a C, an R, and a Go/RGR opsin was a neuralian progenitor.

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http://redwood.berkeley.edu/bruno/animal-eyes/Kaas_revised_2013.pdf

Charles Darwin : On the Origin of Species:

To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I freely confess, absurd in the highest degree. When it was first said that the sun stood still and the world turned round, the common sense of mankind declared the doctrine false; but the old saying of Vox populi, vox Dei, as every philosopher knows, cannot be trusted in science. Reason tells me, that if numerous gradations from a simple and imperfect eye to one complex and perfect can be shown to exist, each grade being useful to its possessor, as is certainly the case; if further, the eye ever varies and the variations be inherited, as is likewise certainly the case; and if such variations should be useful to any animal under changing conditions of life, then the difficulty of believing that a perfect and complex eye could be formed by natural selection, though insuperable by our imagination, should not be considered as subversive of the theory. How a nerve comes to be sensitive to light, hardly concerns us more than how life itself originated; but I may remark that, as some of the lowest organisms, in which nerves cannot be detected, are capable of perceiving light, it does not seem impossible that certain sensitive elements in their sarcode should become aggregated and developed into nerves, endowed with this special sensibility.


How could such a complicated piece of optical machinery arise through a process that has no foresight or intentionality?

When asked, atheists generally point out  to Nillson and Penger's Paper from 1994 ,

where the paper makes following assertion :

http://www.rpgroup.caltech.edu/courses/aph161/Handouts/Nilsson1994.pdf

The evolution of complex structures, however, involves modifications of a large number of separate quantitative characters, and in addition there may be discrete innovations and an unknown number of hidden but necessary phenotypic changes. These complications seem effectively to prevent evolution rate estimates for entire organs and other complex structures. An eye is unique in this respect because the structures necessary for image formation, although there may be several, are all typically quantitative in their nature, and can be treated as local modifications of pre-existing tissues. Taking a patch of pigmented light-sensitive epithelium as the starting point, we avoid the more inaccessible problem of photoreceptor cell evolution. Thus, if the objective is limited to finding the number of generations required for the evolution of an eye’s optical geometry, then the problem becomes solvable.

usually proponents of evolution of the eye come up with that explanation :


Steps in the evolution of the eye as reflected in the range of eye complexity in living mollusk species (left to right): a pigment spot, as in the limpet Patella; a pigment cup, as in the slit shell mollusk Pleurotomaria; the "pinhole-lens" eye of Nautilus; a primitive lensed eye, as in the marine snail Murex; and the complex eye—with iris, crystalline lens, and retina—of octopuses and squids.

http://skeptoid.com/blog/2013/12/24/is-the-human-eye-irreducibly-complex/

Here’s an abbreviated version of the leading model:

A mutation resulted in a single photoreceptor cell, which allowed the organism to respond to light, and helped to calibrate circadian rhythms by detecting daylight.

Over successive generations, possessing multiple photoreceptors became the norm in the gene pool, because individuals with mutations encoding for an increased number of photoreceptors were better able to react to their surroundings. An arms race began, fueling the evolution of the new sensory organ.

Eventually, what was once just a single photoreceptor cell became a light-sensitive patch. At this point, the creature was still only able to distinguish light from dark.

A slight depression in the patch created a pit, for the first time allowing a limited ability to sense from which direction light or shadow was coming from.

The pit’s opening gradually narrowed to create an aperture — like that of a pinhole camera — making vision sharper.

The aqueous humour formed. A colourless, gelatinous mass filling the chamber of the eye, it helped to maintain the shape of the eye and keep the light sensitive retina in place.

A transparent tissue formed at the front, with a concave curvature for refracting light. The addition of this simple lens drastically improved image fidelity.

A transparent layer evolved in front of the lens. This transparent layer, the cornea, further focused light, and also allowed for more blood vessels, better circulation, and larger eyes.

Behind the cornea, a circular ring formed, the iris, with a hole in its centre, the pupil. By constricting, the iris was able to control the amount of light that reached the retina through the pupil.

Separation of these two layers allowed another gelatinous mass to form, the aqueous humor, which further increased refractive power.

http://www.reviewevolution.com/press/pressRelease_EyeEvolution.php

Since Nilsson and Pelger's article was published, it has been widely--but erroneously--reported that their conclusions were based on a computer model. Berlinski calls this claim "an urban myth." At a minimum, PBS should make clear to viewers that Nilsson's conclusions are not based on computer models at all, and it should acknowledge that his work is highly speculative."

http://creationwiki.org/The_eye_is_too_complex_to_have_evolved_%28Talk.Origins%29

http://www.grisda.org/origins/21039.htm

"What is one to make of all this? First, comparing the evolution of the eye to shape changes on a computer screen seems rather far-fetched. The entire project seems closer to an exercise in geometry than in biology. Second, the exercise assumes a functional starting point. Thus it has nothing to do with the origin of the biochemical systems of vision or the requisite neural network. Third, Nilsson and Pelger's computer exercise operates as if each 1% change in morphology can be accounted for by a single gene mutation. They do not consider the effects of pleiotropy, genetic background, or developmental processes. Fourth, an important part of the model relies on the special circumstance of a layer of clear cells covering the "retina." This layer somehow assumes the proper shape of a lens. Fifth, as noted by the authors, several features of the eye remain unaccounted for, such as the iris. Basically, the only result achieved was to show that two light-sensitive surfaces that differ in shape by 1% will have different efficiencies in photoreception, and that an uninterrupted series of 1% improvements is possible. The failure of scientists to produce new structures in selection experiments illustrates the implausibility of Nilsson and Pelger's "just so" story."


http://www.detectingdesign.com/humaneye.html

If a change in selective pressures favored a dimpled eyespot with a slight increase in visual acuity, pretty soon the majority of the population would have dimpled eyespots.  The problem with this notion is that no population of creatures with flat eyespots shows any sort of intra-population range like this were even a small portion of the population has dimpled eyespots to any selectable degree.  This is a common assertion, but it just isn't true.


the eye/brain is howerer  not only a interdependent system:

http://reasonandscience.heavenforum.org/t1638-eye-brain-is-a-interdependent-and-irreducible-complex-system

but the eye is also irreducibly complex in many ways, which can be illustrated best with the Signal transduction pathway in photoreceptor cell's:

http://reasonandscience.heavenforum.org/t1696-photoreceptor-cells



The absorption of light leads to a isomeric change in the retinal molecule.

The signal transduction pathway is the mechanism by which the energy of a photon signals a mechanism in the cell that leads to its electrical polarization. This polarization ultimately leads to either the transmittance or inhibition of a neural signal that will be fed to the brain via the optic nerve. The steps, or signal transduction pathway, in the vertebrate eye's rod and cone photoreceptors are then:

   1.The rhodopsin or iodopsin in the disc membrane of the outer segment absorbs a photon, changing the configuration of a retinal Schiff base cofactor inside the protein from the cis-form to the trans-form, causing the retinal to change shape.

   2.This results in a series of unstable intermediates, the last of which binds stronger to the G protein in the membrane and activates transducin, a protein inside the cell. This is the first amplification step – each photoactivated rhodopsin triggers activation of about 100 transducins. (The shape change in the opsin activates a G protein called transducin.)

   3.Each transducin then activates the enzyme cGMP-specific phosphodiesterase (PDE).

   4.PDE then catalyzes the hydrolysis of cGMP to 5' GMP. This is the second amplification step, where a single PDE hydrolyses about 1000 cGMP molecules.

   5.The net concentration of intracellular cGMP is reduced (due to its conversion to 5' GMP via PDE), resulting in the closure of cyclic nucleotide-gated Na+ ion channels located in the photoreceptor outer segment membrane.

   6.As a result, sodium ions can no longer enter the cell, and the photoreceptor outer segment membrane becomes hyperpolarized, due to the charge inside the membrane becoming more negative.

   7.This change in the cell's membrane potential causes voltage-gated calcium channels to close. This leads to a decrease in the influx of calcium ions into the cell and thus the intracellular calcium ion concentration falls.

   8.A decrease in the intracellular calcium concentration means that less glutamate is released via calcium-induced exocytosis to the bipolar cell (see below). (The decreased calcium level slows the release of the neurotransmitter glutamate, which can either excite or inhibit the postsynaptic bipolar cells.)

   9.Reduction in the release of glutamate means one population of bipolar cells will be depolarized and a separate population of bipolar cells will be hyperpolarized, depending on the nature of receptors (ionotropic or metabotropic) in the postsynaptic terminal (see receptive field).

http://www.detectingdesign.com/humaneye.html

The question now of course is, how could such a system evolve gradually?  All the pieces must be in place simultaneously.  For example, what good would it be for an earthworm that has no eyes to suddenly evolve the protein 11-cis-retinal in a small group or "spot" of cells on its head?  These cells now have the ability to detect photons, but so what?  What benefit is that to the earthworm?  Now, lets say that somehow these cells develop all the needed proteins to activate an electrical charge across their membranes in response to a photon of light striking them.  So what?!  What good is it for them to be able to establish an electrical gradient across their membranes if there is no nervous pathway to the worm's minute brain?   Now, what if this pathway did happen to suddenly evolve and such a signal could be sent to the worm's brain.  So what?!  How is the worm going to know what to do with this signal?  It will have to learn what this signal means.  Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems.  Now the earthworm, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring.  If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them.  All of these wonderful processes need regulation.  No function is beneficial unless it can be regulated (turned off and on).  If the light sensitive cells cannot be turned off once they are turned on, vision does not occur.  This regulatory ability is also very complicated involving a great many proteins and other molecules - all of which must be in place initially for vision to be beneficial.

http://darwins-god.blogspot.com.br/search?q=eye

When in doubt, doubt the data. Paleontologists agree that the fossil record reveals abrupt appearances, but when convenient evolutionists can always protect their theory with those gaps in the fossil record.

Evolutionary thinking is remarkable. I am reminded of John Earman’s remarks about Hume’s arguments. For it is astonishing how well evolution is treated, given how completely the confection collapses under a little probing. So if Benjamin Radford really is interested in why people believe things for which there is little or no evidence, we have just the topic for him.



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http://m.pnas.org/content/103/44/16337.full

Evolution of complexity in signaling pathways

Conclusion

The intuitive view for the emergence of complexity is that it is due to increasing fitness, a view that has found support from studies on digital organisms. However, this study suggests that an imbalance in the effects of size-decreasing and -increasing mutations on function could lead to increase in complexity, supporting a mechanistic or neutral explanation . Hence, as long as there is selection acting on a system, even neutral processes that do not cause any immediate fitness benefit would force the system toward higher complexity.

We find that the amount of the aforementioned imbalance is related to complexity itself. It is highest for the simplest possible pathways that could achieve the task for which there is selection operating and decreases with increasing complexity. Hence, as evolution progresses, pathways achieve a certain size or level of complexity that is always well above the minimum required for their function. Further, we find that although simulations with different selection criteria start with pathways of the same size, for pathways that are under selection for functions that are attainable by many different topologies (i.e., that are simpler to achieve), the final level of complexity achieved tends to be higher.

These findings have implications for our understanding of the evolution of new features. For example, in simulating the evolution of a random population of three-protein pathways under selection for responding to a given signal, we reach a structurally diverse population with an average pathway size of ≈14 proteins. Given the exponential relation between pathway size and available pathway topologies, it is plausible to assume that such growth would facilitate the emergence of pathways with various response dynamics that would not have been possible with three proteins only. If such pathways achieve new functions or high-fitness solutions under the current selection criterion, they would be strongly selected. Hence, even though complexity can emerge neutrally, once it results in evolutionary favorable pathways, it may be maintained subsequently by selection.

Finally, we note that the presented results have an interesting connection to robustness. In general, robustness in biological pathways is associated with the ability of such pathways to withstand knockout mutations or disturbances in interaction parameters. Based on this description, many natural pathways have been found to have high robustness (19–24). This observation becomes obvious in light of the presented results. Our simulations suggest that in general, simplest-solution pathways are nonrobust toward deletions. Thus, populations predominantly consisting of such pathways drift toward larger, more complex solutions, and, in this sense, selection for function leads to emergence of robustness. A similar scenario is given for the evolution of robustness in general (25); through evolutionary mechanisms populations move toward wide plateaus on an imaginary fitness landscape, where they would be protected against small perturbations (i.e., they have high robustness). The idea of an imbalance between the functional effects of various mutations having different effects could be seen as the driving force behind such move, leading both to high robustness and high complexity. This statement overlaps with the theories that see complexity and robustness tying closely together (26).

The presented discussion approximates the behavior of biological pathways with a simple mathematical model and makes several assumptions regarding the nature and rate of mutations affecting their structure. Although the true nature of these pathways clearly is more complicated, we believe that the qualitative conclusions of this theoretical study would remain under biologically relevant parameter values (see Methods). These conclusions could also be extendable to any system that is under selection and is subject to mutations affecting its structure. Under such conditions, the idea of complexity arising neutrally could be more general.

intuitive view

this description is highly unspecific.... typical scientific wishi washi smart seeming, but baseless in essence.

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11 The Irreducible Complexity of Sight on Sun Jul 20, 2014 6:11 am

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The Irreducible Complexity of Sight

http://reasonandscience.heavenforum.org/t1638-eye-brain-is-a-interdependent-and-irreducible-complex-system#3058

and

The Inference to Design

Thesis by Wayne Talbot

Our sense of sight is best explained by intelligent design: the system is irreducibly complex and the prerequisites for processing visual information are beyond development by undirected biological processes.

Propositions:

1. The origin of knowledge and information in the brain cannot be explained by undirected organic processes.
2. Sight is the result of intelligent data processing.
3. Data input requires a common understanding between sender and receiver of the data coding and transmission protocols.
4. Data storage and retrieval requires an understanding of the data from an informational perspective.
5. Data processing requires meta-data: conceptual and contextual data to be pre-loaded prior to the input of transaction data.
6. Light can be considered an encoded data stream which is decoded and re-encoded by the eye for transmission via the optic nerve to serve as input data.
7. All data transmissions are meaningless without the superimposition of meta-data.
8. None of the components of our visual system individually offer any advantage for natural selection.

The Concepts of Light and Sight

Imagine that some thousands of years ago, a mountain tribe suffered a disease or mutation such that all members became blind. Generation after generation were born blind and eventually even the legends of the elders of being able to see were lost. Everyone knew that they had these soft spots in their heads which hurt when poked, but nobody knew if they had some intended function. Over time, the very concepts of light and sight no longer existed within their tribal knowledge. As a doctor specialising in diseases and abnormalities of the eye, you realise that with particular treatment you can restore the sight of these people. Assuming that you are fluent in the local language, how would you describe what you can do for them? How would you convey the concept of sight to people to whom such an idea was beyond their understanding?
My point is that this is the very problem that primitive organisms would have faced if sight did in fact evolve organically in an undirected fashion. When the first light sensitive cell hypothetically evolved, the organism had no way of understanding that the sensation it experienced represented light signals conveying information about its environment: light and sight were concepts unknown to it.

The Training of Sight

Those familiar with the settlement of Australia by Europeans in the 19th century, and the even earlier settlements in the Americas and Africa would have heard of the uncanny ability of the indigenous population to track people and animals. It was not so much that their visual acuity was better, but that they had learned to understand what they were seeing. It was found that this tracking ability could be taught and learned. In military field craft, soldiers are taught to actively look for particular visual clues and features. In my school cadet days, we undertook night “lantern stalks” (creeping up on enemy headquarters) and later in life, the lessons learned regarding discrimination of objects in low light were put to good use in orienteering at night. All of this experience demonstrates that while many people simply “see” passively, it is possible to engage the intellect and actively “look”, thus seeing much more.

With the advent of the aeroplane came aerial photography and its application during wartime as a method of intelligence gathering. Photographic analysis was a difficult skill to acquire - many people could look at the same picture but offer differing opinions as to what they were seeing, or rather thought they were seeing.
The underlying lesson is that sight is as much a function of intellect as it is receiving light signals through the eyes. Put another way, it is intelligent data processing.
Understanding Data vs Information

The digital computer was invented circa 1940 and during the technical revolution that followed, we have come to learn a great deal about information processing. I was fortunate to join the profession in the very early days of business computing and through training and experience, acquired an understanding of data coding methodologies, their application and interpretation. More importantly however, I came to understand a great deal about how data becomes information, and when it isn’t. In the early days of sequential and index-sequential files, the most common programming error occurred in attempting to match master, application (reference), and transaction files. With the advent of direct access files and disk resident databases, new skills were required in the fields of data analysis, data structuring, and data mining.

The computing experience teaches this: data only becomes cognitive information when intelligently processed against a pre-loaded referential framework of conceptual and contextual data. Using this computer analogy, master files represented conceptual information, application files provided context, and input data was provided by transaction files.
With apologies to Claude Shannon, Werner Gitt and other notables who have contributed so much to our understanding on this subject, I would contend that in the context of this discussion, none of these files contain information in the true sense: each contains data which only becomes usable information when intelligently correlated. I would further contend that no single transmission in any form can stand alone as information: absent of a preloaded conceptual and contextual framework in the recipient, it can only ever be a collection of meaningless symbols. This is easily demonstrated by simply setting down everything you have to know before you can read and understand these words written here, or what you would have to know before reading a medical journal in a foreign language in an unfamiliar script such as Hebrew or Chinese.

Can Coding Systems Evolve?

A computer processor operates via switches set to either “on” or “off”. A system with 8 switches (28) provides 256 options; 16 switches (216) 65,536; 32 switches (232) 4,294,967,296; and 64 switches (264) the very massive 18 trillion. This feature provides the terminology such as 32-bit and 64-bit computers: it refers to the number of separate addresses than can be accessed in memory. In the early days of expensive iron-core memory, 8 or 16 bit addressing was adequate, but with the development of the silicon chip and techniques for dissipating heat, larger memory became viable thus requiring greater addressing capability and the development of 32 then 64-bit computers. All very interesting, you may say but why is that relevant? The relevance is found in most users’ experience: software versions that are neither forward nor backward compatible. The issue is that as coding systems change or evolve, the processing and storage systems cannot simply evolve in an undirected fashion: they must be intelligently converted. Let us look at some practical examples.

Computer coding systems are multi-layered. The binary code (1’s and 0’s) of computers translates to a coded language such as Octal through to ASCII, or Hexadecimal through to EBCDIC, and then to a common human language such as English or French. Computer scientists long ago established these separate coding structures for reasons not relevant here. The point to note is that in general, you cannot go from Octal to EBCDIC or from Hexadecimal to ASCII: special intermediate conversion routines are needed. The problem is that once coding systems are established, particularly multi-layered systems, any sequence of symbols which does not conform to the pattern cannot be processed without an intelligent conversion process.

Slightly off-topic, but consider the four chemicals in DNA which are referred to as A, C, G, and T. Very recently, scientists expressed surprise in finding that the DNA sequences code not just for proteins, but for the processing of these proteins. In other words, there is not just one but two or more “languages” written into our genome. What surprises me is that they were surprised: I would have thought the multi-language function to be obvious, but I will leave that for another time. If an evolving genome started with just two chemicals, say A and C, downstream processes could only recognise combinations of these two. If a third chemical G arose, there would be no system that could utilise it and more probably, its occurrence would interfere in a deleterious way. Quite simply, you cannot go from a 2 letter code to a 3 letter code without re-issuing the code book, a task quite beyond undirected biological evolution.

The Code Book Enigma

I will use an example similar to DNA because it is much easier to illustrate the problem using a system comprising just four symbols, in this case W, X, Y, and Z. I am avoiding ACGT simply so that you are not distracted by your knowledge of that particular science. Our coding system uses these 4 letters in groups of 3. If I sent you the message “XYW ZWZ YYX WXY” you would have no idea of what it means: it could be a structured sequence or a random arrangement, the letters are just symbols which are individually meaningless until intelligently arranged in particular groups or sequences. To be useful, we would need to formalise the coding sequences in a code book: that way the sender can encode the message and someone with the same version of the code book can decode the message and communication is achieved. Note that if the sender and receiver are using different versions of the code book, communication is compromised.
This brings us to a vital concept: meta-data (or data about data).
There is a foundational axiom that underpins all science and intellectual disciplines––nothing can explain itself. The explanation of any phenomenon will always lie outside itself, and this applies equally to any coding system: it cannot explain itself. You may recall the breakthrough achieved by archaeologists in deciphering Egyptian hieroglyphs when they found the Rosetta Stone.

In our example, the code book provides the meta-data about the data in the encoded message. Any language, particularly one limited to just four letters, requires a code book to both compose and decipher the meaning. Every time there is a new rearrangement of the letters, or new letters are added to (or deleted from) an existing string, the code book has to be updated. From a chronological sequence perspective, for a change to be useful, the code explanation or definition must precede, not follow, any new arrangement of letters in a message. Rearrangements that occur independently of the code book cannot be understood by downstream processes. Logically, the code book is the controlling mechanism, not the random rearrangements of coding sequences. First the pre-arranged code sequence, then its implementation. In other words, it is a top-down process, not the bottom-up process that evolutionists such as Richard Dawkins assert.
Now it matters not whether you apply this to the evolution of the genome or to the development of our senses, the same principle holds: ALL data must be preceded by meta-data to be comprehensible as information. In general, messages or other forms of communication can be considered as transactions which require a conceptual and contextual framework to provide meaning.

Understanding Input Devices


We have five physical senses: sight, hearing, smell, taste, and touch, and each requires unique processes, whether physical and/or chemical. What may not be obvious from an evolution standpoint is that for the brain to process these inputs, it must first know about them (concept) and how to differentiate amongst them (context). Early computers used card readers as input devices, printers for output, and magnetic tape for storage (input & output). When new devices such as disk drives, bar code readers, plotters, etc were invented, new programs were needed to “teach” the central processor about these new senses. Even today, if you attach a new type of reader or printer to your computer, you will get the message “device not recognised” or similar if you do not preload the appropriate software. It is axiomatic that an unknown input device cannot autonomously teach the central processor about its presence, its function, the type of data it wishes to transmit, or the protocol to be used.
The same lessons apply to our five senses. If we were to hypothesise that touch was the first sense, how would a primitive brain come to understand that a new sensation from say light was not just a variation of touch?

Signal Processing

All communications can be studied from the perspective of signal processing, and without delving too deeply, we should consider a just few aspects of the protocols. All transmissions, be they electronic, visual, or audible are encoded using a method appropriate to the medium. Paper transmissions are encoded in language using the symbol set appropriate for that language; sound makes use of wavelength, frequency and amplitude; and light makes use of waves and particles in a way that I cannot even begin to understand. No matter, it still seems to work. The issue is that for communication to occur, both the sender and receiver must have a common understanding of the communication protocol: the symbols and their arrangement, and both must have equipment capable of encoding and decoding the signals.
Now think of the eye. It receives light signals containing data about size, shape, colour, texture, brightness, contrast, distance, movement, etc. The eye must decode these signals and re-encode them using a protocol suitable for transmission to the brain via the optic nerve. Upon receipt, the brain must store and correlate the individual pieces of data to form a mental picture, but even then, how does it know what it is seeing? How did the brain learn of the concepts conveyed in the signal such as colour, shape, intensity, and texture? Evolutionists like to claim that some sight is better than no sight, but I would contend that this can only be true provided that the perceived image matches reality: what if objects approaching were perceived as receding? Ouch!

When the telephone was invented, the physical encode/decode mechanisms were simply the reverse of one another, allowing sound to be converted to electrical signals then reconverted back to sound. Sight has an entirely different problem because the encode mechanism in the eye has no counterpart in the brain: the conversion is to yet another format for storage and interpretation. These two encoding mechanisms must have developed independently, yet had to be coherent and comprehensible with no opportunity for prolonged systems testing. I am not a mathematician, but the odds against two coding systems developing independently yet coherently in any timespan must argue against it ever happening.

Data Storage and Retrieval

Continuing our computer analogy, our brain is the central processing unit and just as importantly, our data storage unit, reportedly with an equivalent capacity of 256 billion gigabytes (or thereabouts). In data structuring analysis, there is always a compromise to be made between storage and retrieval efficiency. The primary difference from an analysis perspective is whether to establish the correlations in the storage structure thus optimising the retrieval process, or whether to later mine the data looking for the correlations. In other words, should the data be indexed for retrieval rather than just randomly distributed across the storage device. From our experience in data analysis, data structuring, and data mining, we know that it requires intelligence to structure data and indices for retrieval, and even greater intelligence to make sense of unstructured data.
Either way, considerable understanding of the data is required.
Now let’s apply that to the storage, retrieval, and processing of visual data. Does the brain store the data then analyse, or analyse and then store, all in real time? Going back to the supposed beginnings of sight, on what basis did the primitive brain decide where to store and how to correlate data which was at that time, just a meaningless stream of symbols? What was the source of knowledge and intelligence that provided the logic of data processing?

Correlation and Pattern Recognition

In the papers that I have read on the subject, scientists discuss the correlation of data stored at various locations in the brain. As best as I understand it, no-one has any idea of how or why that occurs. Imagine a hard drive with terabytes of data and those little bits autonomously arranging themselves into comprehensible patterns. Impossible you would assert, but that is what evolution claims. It is possible for chemicals to self-organise based on their physical properties, but what physical properties are expressed in the brain’s neural networks such that self-organisation would be possible? I admit to very limited knowledge here but as I understand it, the brain consists of neurons, synapses, and axons, and in each class, there is no differentiation: every neuron is like every other neuron, and so forth. Now even if there are differences such as in electric potential, the differences must occur based on physical properties in a regulated manner for there to be consistency. Even then, the matter itself can have no “understanding” of what those material differences mean in terms of its external reality.

In the case of chemical self-organisation, the conditions are preloaded in the chemical properties and thus the manner of organisation is pre-specified. When it comes to data patterns and correlation however, there are no pre-specified properties of the storage material that are relevant to the data which is held, whether the medium be paper, silicon, or an organic equivalent. It can be demonstrated that data and information is independent of the medium in which it is stored or transmitted, and is thus not material in nature. Being immaterial, it cannot be autonomously manipulated in a regulated manner by the storage material itself, although changes to the material can corrupt the data.
Pattern recognition and data correlation must be learned, and that requires an intelligent agent that itself is preloaded with conceptual and contextual data.
Facial Recognition

Facial recognition has become an important tool for security and it is easy for us to think, “Wow! Aren’t computers smart!” The “intelligence” of facial recognition is actually an illusion: it is an algorithmic application of comparing data points but what the technology cannot do is identify what type of face is being scanned. In 2012, Google fed 10 million images of cat faces into a very powerful computer system designed specifically for one purpose: that an algorithm could learn from a sufficient number of examples to identify what was being seen. The experiment was partially successful but struggled with variations in size, positioning, setting and complexity. Once expanded to encompass 20,000 potential categories of object, the identification process managed just 15.8% accuracy: a huge improvement on previous efforts, but nowhere near approaching the accuracy of the human mind.

The question raised here concerns the likelihood of evolution being able to explain how facial recognition by humans is so superior to efforts to date using the best intelligence and technology.

Irreducible Complexity

Our sense of sight has many more components than described here. The eye is a complex organ which would have taken a considerable time to evolve, the hypothesis made even more problematic by the claim that it happened numerous times in separate species (convergent evolution). Considering the eye as the input device, the system requires a reliable communications channel (the optic nerve) to convey the data to the central processing unit (the brain) via the visual cortex, itself providing a level of distributed processing. This is not the place to discuss communications protocols in detail, but very demanding criteria are required to ensure reliability and minimise data corruption. Let me offer just one fascinating insight for those not familiar with the technology. In electronic messaging, there are two basic ways of identifying a particular signal: (1) by the purpose of the input device, or (2) by tagging the signal with an identifier.

A certain amount of signal processing occurs in the eye itself; particular receptor cells have been identified in terms of function: M cells are sensitive to depth and indifferent to color; P cells are sensitive to color and shape; K cells are sensitive to color and indifferent to shape or depth. The question we must ask is how an undirected process could inform the brain about these different signal types and how they are identified. The data is transmitted to different parts of the brain for parallel processing, a very efficient process but one that brings with it a whole lot of complexity. The point to note is that not only does the brain have the problem of decoding different types of messages (from the M, P, and K cells), but it has to recombine this data into a single image, a complex task of co-ordinated parallel processing.
Finally we have the processor itself which if the evolution narrative is true, progressively evolved from practically nothing to something hugely complex. If we examine each of the components of the sight system, it is difficult to identify a useful function for any one of them operating independently except perhaps the brain. However, absent of any preloaded data to interpret input signals from wherever, it is no more useful than a computer without an operating system. It can be argued that the brain could have evolved independently for other functions, but the same argument could not be made for those functions pertaining to the sense of sight.
As best as I can understand, our system of sight is irreducibly complex.

Inheriting Knowledge

Let us suppose, contrary to all reason and everything that we know about how knowledge is acquired, that a primitive organism somehow began developing a sense of sight. Maybe it wandered from sunlight into shadow and after doing that several times, came to “understand” these variations in sensation as representative of its external environment, although just what it understood is anyone’s guess, but let us assume that it happened. How is this knowledge then inherited by its offspring for further development? If the genome is the vehicle of inheritance, then sensory experience must somehow be stored therein.
I have no answer to that, but I do wonder.
Putting it all together
I could continue to introduce even greater complexities that are known to exist, but I believe that we have enough to draw some logical conclusions. Over the past sixty years, we have come to understand a great deal about the nature of information and how it is processed. Scientists have been working on artificial intelligence with limited success, but it would seem probable that intelligence and information can only be the offspring of a higher intelligence. Even where nature evidences patterns, those patterns are the result of inherent physical properties, but the patterns themselves cannot be externally recognised without intelligence. A pattern is a form of information, but without an understanding of what is regular and irregular, it is nothing more than a series of data points.

We often hear the term, emergent properties of the brain, to account for intelligence and knowledge, but just briefly, what is really meant is emergent properties of the mind. You may believe that the mind is nothing more than a description of brain processes but even so, emergence requires something from which to emerge, and that something must have properties which can be foundational to the properties of that which emerges. Emergence cannot explain its own origins, as we have noted before.
Our system of sight is a process by which external light signals are converted to an electro-chemical data stream which is fed to the brain for storage and processing. The data must be encoded in a regulated manner using a protocol that is comprehensible by the recipient. The brain then stores that data in a way that allows correlation and future processing. Evolutionists would have us believe that this highly complex system arose through undirected processes with continual improvement through generations of mutation and selection. However, there is nothing in these processes which can begin to explain how raw data received through a light sensitive organ could be processed without the pre-loading of the meta-data that allows the processor to make sense of the raw data. In short, the only source of data was the very channel that the organism neither recognised nor understood.

Without the back-end storage, retrieval, and processing of the data, the input device has no useful function. Without an input device, the storage and retrieval mechanisms have no function. Just like a computer system, our sensory sight system is irreducibly complex.

Footnote:

Earlier I noted that I was surprised that scientists were surprised to find a second language in DNA, but on reflection I considered that I should justify that comment. The majority of my IT career was in the manufacturing sector. I have a comprehensive understanding of the systems and information requirements of manufacturing management, having designed, developed, and implemented integrated systems across a number of vertical markets and industries.
The cell is often described as a mini factory and using that analogy, it seems logical to me that if the genome holds all of the production data in DNA, then it must include not just the Bill of Material for proteins, but also the complete Bill of Resources for everything that occurs in human biology and physiology. Whether that is termed another language I will leave to others, but what is obvious to anyone with experience in manufacturing management is that an autonomous factory needs more information than just a recipe.
Fred Hoyle’s “tornado through a junk yard assembling a Boeing 747” analogy understates the complexity by several orders of magnitude. A more accurate analogy would be a tornado assembling a full automated factory capable of replicating itself and manufacturing every model of airplane Boeing ever produced.

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Did eyes evolve by Darwinian mechanisms? 1

The simplest eye type known is the ocellus, a multicellular eye comprising of photoreceptor cells, pigment cells and nerve cells to process the information—is step 4 in Darwin’s list.27 The most primitive eye that meets the definition of an eye is the tiny—about the size of the head of a pin—microscopic marine crustacean copepod copilia. Only the females possess what Wolken and Florida call ‘remarkable eyes which make up more than half of its transparent body.’28 Claimed to be a link between an eyespot and a more complex eye, it has two exterior lenses that raster like a scanning electron microscope to gather light that is processed and then sent to its brain.29 It has retinal cells and an eye ‘analogous to a superposition-type ommatidium of compound eyes’.30 This, the most primitive true eye known, is at stage 6 of Darwin’s evolutionary hierarchy!

Dennett wrote that the eye lens is ‘exquisitely well-designed to do its job, and the engineering rationale for the details is unmistakable, but no designer ever articulated it.’44 He concludes that its design is not real, but an illusion because evolution explains the eye without the need for a designer. This review has shown that evolution does not explain the existence of the vision system, but an intelligent designer does. The leading eye evolution researchers admit they only ‘have some understanding of how eyesmight have evolved’.45 These explanations do not even scratch the surface of how a vision system could have arisen by evolution—let alone ‘when’.
Much disagreement exists about the hypothetical evolution of eyes, and experts recognize that many critical problems exist. Among these problems are an explanation of the evolution of each part of the vision system, including the lens, the eyeball, the retina, the entire optical system, the occipital lobes of the brain, and the many accessory structures. Turner stressed that ‘the real miracle [of vision] lies not so much in the optical eye, but in the computational process that produces vision.’46 All of these different systems must function together as an integrated unit for vision to be achieved. As Arendt concludes, the evolution of the eye has been debated ever since Darwin and is still being debated among Darwinists.47 For non-evolutionists there is no debate.





1) http://creation.com/did-eyes-evolve-by-darwinian-mechanisms[/size][/size][/size][/size][/size][/size]

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How the origin of the human eye is best explained through intelligent design  1

http://reasonandscience.heavenforum.org/t1638-eye-brain-is-a-interdependent-and-irreducible-complex-system#5103



The human eye consists of over two million working parts making it second only to the brain in complexity. Evolutionists believe that the human eye is a product of millions of years of mutations and natural selection. As you read about the amazing complexity of the eye please ask yourself: could this really be a product of evolution?

Automatic focus


The lens of the eye is suspended in position by hundreds of string like fibres called Zonules. The ciliary muscle changes the shape of the lens. It relaxes to flatten the lens for distance vision; for close work it contracts rounding out the lens. This happens automatically and instantaneously without you having to think about it.
How could evolution produce a system that even knows when it is in focus? Let alone the mechanism to focus.
How would evolution produce a system that can control a muscle that is in the perfect place to change the shape of the lens?


A visual system


The retina is composed of photoreceptor cells. When light falls on one of these cells, it causes a complex chemical reaction that sends an electrical signal through the optic nerve to the brain. It uses a signal transduction pathway, consisting of 9 irreducible steps. the light must go all the way through. Now, what if this pathway did happen to suddenly evolve and such a signal could be sent and go all the way through.  So what?!  How is the receptor cell going to know what to do with this signal?  It will have to learn what this signal means.  Learning and interpretation are very complicated processes involving a great many other proteins in other unique systems.  Now the cell, in one lifetime, must evolve the ability to pass on this ability to interpret vision to its offspring.  If it does not pass on this ability, the offspring must learn as well or vision offers no advantage to them.  All of these wonderful processes need regulation.  No function is beneficial unless it can be regulated (turned off and on).  If the light sensitive cells cannot be turned off once they are turned on, vision does not occur.  This regulatory ability is also very complicated involving a great many proteins and other molecules - all of which must be in place initially for vision to be beneficial. How does evolution explain our retinas having the correct cells which create electrical impulses when light activates them?

Making sense of it all




Each eye takes a slightly different picture of the world. At the optic chiasm each picture is divided in half. The outer left and right halves continue back toward the visual cortex. The inner left and right halves cross over to the other side of the brain then continue back toward the visual cortex.Also, the image that is projected onto the retina is upside down. The brain flips the image back up the right way during processing. Somehow, the human brain makes sense of the electrical impulses received via the optic nerve. The brain also combines the images from both eyes into one image and flips it up the right way… and all this is done in real time. How could  natural selection recognize the problem and evolve the mechanism of  the left side of the brain receiving the information from the left side of both eyes and the right side of the brain taking the information from the right side of both eyes? How would evolution produce a system that can interpret electrical impulses and process them into images? Why would evolution produce a system that knows the image on the retina is upside down?

Constant level of light


The retina needs a fairly constant level of light intensity to best form useful images with our eyes. The iris muscles control the size of the pupil. It contracts and expands, opening and closing the pupil, in response to the brightness of surrounding light. Just as the aperture in a camera protects the film from over exposure, the iris of the eye helps protect the sensitive retina. How would evolution produce a light sensor? Even if evolution could produce a light sensor.. how can a purely naturalistic process like evolution produce a system that knows how to measure light intensity? How would evolution produce a system that would control a muscle which regulates the size of the pupil?

Detailed vision


Cone cells give us our detailed color daytime vision. There are 6 million of them in each human eye. Most of them are located in the central retina. There are three types of cone cells: one sensitive to red light, another to green light, and the third sensitive to blue light.
Isn’t it fortunate that the cone cells are situated in the centre of the retina? Would be a bit awkward if your most detailed vision was on the periphery of your eye sight?


Night vision


Rod cells give us our dim light or night vision. They are 500 times more sensitive to light and also more sensitive to motion than cone cells. There are 120 million rod cells in the human eye. Most rod cells are located in our peripheral or side vision. it can modify its own light sensitivity. After about 15 seconds in lower light, our bodies increase the level of rhodopsin in our retina. Over the next half hour in low light, our eyes get more an more sensitive. In fact, studies have shown that our eyes are around 600 times more sensitive at night than during the day. Why would the eye have different types of photoreceptor cells with one specifically to help us see in low light?

Lubrication


The lacrimal gland continually secretes tears which moisten, lubricate, and protect the surface of the eye. Excess tears drain into the lacrimal duct which empty into the nasal cavity.
If there was no lubrication system our eyes would dry up and cease to function within a few hours.
If the lubrication wasn’t there we would all be blind. Had this system not have to be fully setup from the beginning?
Fortunate that we have a lacrimal duct aren’t we? Otherwise we would have steady stream of tears running down our faces!


Protection


Eye lashes protect the eyes from particles that may injure them. They form a screen to keep dust and insects out. Anything touching them triggers the eyelids to blink.
How is it that the eyelids blink when something touches the eye lashes?


Operational structure


Six muscles are in charge of eye movement. Four of these move the eye up, down, left and right. The other two control the twisting motion of the eye when we tilt our head.
The orbit or eye socket is a cone-shaped bony cavity that protects the eye. The socket is padded with fatty tissue that allows the eye to move easily. When you tilt your head to the side your eye stays level with the horizon.. how would evolution produce this? Isn’t it amazing that you can look where you want without having to move your head all the time? If our eye sockets were not padded with fatty tissue then it would be a struggle to move our eyes.. why would evolution produce this?


Poor Design?


Some  have claimed that the eye is wired back to front and therefore it must be the product of evolution. They claim that a designer would not design the eye this way. Well, it turns out this argument  stems from a lack of knowledge.

The idea that the eye is wired backward comes from a lack of knowledge of eye function and anatomy.
Dr George Marshall

Dr Marshall explains that the nerves could not go behind the eye, because that space is reserved for the choroid, which provides the rich blood supply needed for the very metabolically active retinal pigment epithelium (RPE). This is necessary to regenerate the photoreceptors, and to absorb excess heat. So it is necessary for the nerves to go in front instead.

The more I study the human eye, the harder it is to believe that it evolved. Most people see the miracle of sight. I see a miracle of complexity on viewing things at 100,000 times magnification. It is the perfection of this complexity that causes me to baulk at evolutionary theory.
Dr George Marshall

Evolution of the eye?


Proponents of evolutionary mechanisms have come up with how they think the eye might have gradually evolved over time but it’s nothing more than speculation.
For instance, observe how Dawkins explains the origin of the eye:

https://www.youtube.com/watch?v=sUjd8x-1xM0


Observe the words ‘suppose’, ‘probably’, ‘suspect’, ‘perhaps’ & ‘imagine’? This is not science but pseudo scientific speculation and story telling. Sure, there are a lot of different types of eyes out there but that doesn’t mean they evolved. Besides, based on the questions above you can see how much of an oversimplification Dawkins presentation is.

Conclusion


The human eye is amongst  the best automatic camera in existence. Every time we change where we’re looking, our eye (and retina) is changing everything else to compensate: focus & light intensity are constantly adjusting to ensure that our eyesight is as good it can be. Man has made his own cameras… it took intelligent people to design and build them. The human eye is better than the best human made camera. How is the emergence of eyes best explained, evolution, or design ?!

1. http://web.archive.org/web/20160322111142/http://goddidit.org/the-human-eye

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